In-vitro fatigue and fracture performance of three different ferrulized implant connections used in fixed prosthesis.

BACKGROUND/PURPOSE: The aim of the present in vitro study was to evaluate fatigue resistance of dental fixtures in three different types of fixture/abutment finishing line. MATERIALS AND METHODS: Transmucosal dental implants, with or without ferrulized neck, underwent fatigue tests (static and dynamic load) using the following standard protocol: UNI EN ISO 14801:2016. Two types of loading devices (screw- or cement-retained restoration) were also tested, and fatigue cycle tests were run to failure. Data of static and dynamic load tests were analyzed by proper statistical methods. RESULTS: Following standard protocol for fatigue testing, the ILC type (Implant Level with ferrulized neck and cement-retained crown) showed a non-significant but higher Ultimate Failure Load (UFL = 445.7 N) compared to AL type (Abutment Level without ferrule effect, 421.6 N) and ILS type (Implant Level with ferrulized neck and Screw-retained crown, 362.8 N). No fracture of the titanium-base was registered in the tested specimens during the static loadings. Permanent deformations of the materials were observed. CONCLUSION: The number of cycles to either fracture or deformation (higher than 4 mm) occurring during fatigue tests showed that the stress rupture curve of the materials in group ILS appeared to be significantly different from those of the ILC and AL groups (p-values < 0.01): much higher life of one-half order of magnitude.

SerpinB3 induces dipeptidyl-peptidase IV/CD26 expression and its metabolic effects in hepatocellular carcinoma.

AIMS: In hepatocellular carcinoma (HCC), the regulatory protease Dipeptidyl-peptidase IV (DPPIV/CD26), that possesses pro-apoptotic properties, has been found abnormally regulated. The protease inhibitor SerpinB3, exerting anti-apoptotic activity, has also been described to be upregulated, especially in HCCs with poor prognosis. The aim of this study was to investigate the possible relationship between these two molecules in HCC patients and in experimental models. MATERIALS AND METHODS: DPPIV/CD26 and SerpinB3 expression was measured in liver specimens of 67 patients with HCC. HepG2 and Huh7 cells, stably transfected to overexpress SerpinB3, and respective control cells were used to assess biological and metabolic modifications of DPPIV/CD26 activity induced by this serpin. KEY FINDINGS: DPPIV/CD26 and SerpinB3 were localized in the same tumoral areas and both molecules were correlated with the grade of tumor differentiation, with the highest values detected in GI tumors. Cell lines over-expressing SerpinB3 displayed upregulation of DPPIV/CD26, likely as a feedback mechanism, due to the DPPIV/CD26 protease activity inhibition by SerpinB3, as confirmed by the similar behavior induced by the inhibitor Sitagliptin. Moreover, they exhibited lower glycogen storage and higher lipid accumulation, typical effects of DPPIV/CD26. SIGNIFICANCE: A close connection between SerpinB3 and DPPPIV has been identified, but further studies are required to better understand the mechanism by which these proteins communicate and exert metabolic effects in HCC.